肥胖多囊卵巢综合征患者血脂异常的相关危险因素分析

目的比较肥胖多囊卵巢综合征(PCOS)与肥胖非PCOS患者血脂水平及体脂分布差异,探究肥胖PCOS患者脂代谢异常的特点及影响因素。方法回顾性分析2017年12月至2018年6月就诊于盛京医院内分泌科的86例门诊患者,其中56例肥胖PCOS患者为肥胖PCOS组,30例匹配年龄、体重指数(BMI)的肥胖非PCOS患者为肥胖非PCOS组。检测身高、体重、内脏脂肪面积、血脂、性激素、甲状腺功能、hsCRP、空腹血糖及胰岛素水平,比较两组患者的代谢相关指标及激素水平,并做指标间的相关性分析。结果肥胖PCOS组血浆总胆固醇(TC)、低密度脂蛋白(LDL)、载脂蛋白B(ApoB)、LH、FSH、LH/FSH、睾酮(T)、游离雄激素指数(FAI)高于肥胖非PCOS组,血清游离甲状腺素(FT4)低于肥胖非PCOS组,均有统计学差异(P<0.05)。T、FAI、LH、FSH与TC呈正相关,T、LH与LDL呈正相关,T与ApoB呈正相关(P均<0.05)。肥胖PCOS组内脏脂肪面积、BMI与腰围之间两两呈正相关,腰围、BMI均与胰岛素抵抗指数(HOMA-IR)、超敏C反应蛋白(hsCRP)呈正相关,内脏脂肪面积与T呈正相关,甘油三酯(TG)与FAI呈正相关,HDL与hsCRP呈负相关(P均<0.05)。结论肥胖PCOS患者血脂异常程度比普通肥胖患者更严重,血清TC、LDL、ApoB水平显著升高,高雄激素可能是导致血脂差异的重要原因之一。与肥胖相关的慢性炎症状态也在一定程度上引起脂代谢紊乱,可以通过减重有效缓解肥胖PCOS患者的血脂异常。     

多囊卵巢综合征的治疗

多囊卵巢综合征 (polycystic ovary syn-drome,PCOS)是一种生育年龄妇女常见的内分泌及糖代谢异常所致的病理状态 ,以雄激素过多及长期无排卵为特征。 1 93 5年 Stein及L eventhal将 3 4年间收集的 1 0 8例典型病例 ,归纳为闭经、多毛、肥胖及不孕等四大症状 ,称之为 Stein及 L eventhal(S-L)综合征。近数十年来 ,由于临床实践及各种实验研究不断深入 ,使人们对 PCOS的认识不断深入 ,S-L综合征的定义已远不适用于 PCOS[1] ,不断有新的观点和技术出现。由于雄激素过多而出现多毛、痤疮等现象 ,多数病人体态肥胖 ,无论肥胖与否 ,均有…     

调整生活方式对多囊卵巢综合征女性妊娠结局的影响

多囊卵巢综合征(PCOS)是育龄期女性最常见的生殖内分泌疾病,临床表现具有异质性,包括肥胖、不规律排卵或无排卵、不孕、月经失调以及雄激素过多、胰岛素抵抗等。肥胖PCOS女性不仅表现出生殖功能下降、代谢综合症发生风险增加,而且其心理健康及生活质量也受到极大影响。助孕前通过饮食及运动疗法等生活方式干预减重,有利于恢复自主排卵功能、提高自然妊娠率,提高助孕治疗的妊娠率及活产率,降低妊娠并发症风险,从而改善妊娠结局。本文将从PCOS临床特征,调整生活方式的实施、临床意义及相关机制,调整生活方式改善肥胖PCOS女性妊娠结局等方面进行综述。     

多囊卵巢综合征与脂肪因子相关性的研究进展

多囊卵巢综合征(polycystic ovary syndrome,PCOS)是育龄期妇女最常见的一种内分泌及代谢紊乱性疾病,其主要特征为肥胖、胰岛素抵抗、高雄激素表现、持续性无排卵以及卵巢多囊样改变等。近年来发现肥胖与PCOS的发生有着密切的联系,随着对脂肪细胞的内分泌作用进一步了解,逐渐认识到脂肪所产生的脂肪细胞因子可能是导致PCOS发生的重要因素之一。现就国内外这一方面的研究进展做一综述。     

胰岛素抵抗与多囊卵巢综合征

多囊卵巢综合征(PCOS)是妇科常见的内分泌疾病,其发病机理可能涉及下丘脑、垂体、肾上腺、胰岛素抵抗、肥胖等多种因素。国外对胰岛素抵抗的研究较多,现就胰岛素抵抗与PCOS进行综述。     

多囊卵巢综合征患者卵巢黄素化颗粒细胞瘦素信号转导分子STAT3磷酸化表达的研究

目的检测多囊卵巢综合征(PCOS)患者卵巢黄素化颗粒细胞瘦素信号转导子和活化子STAT3磷酸化(p-STAT3)水平,并观察瘦素体外对培养卵巢黄素化颗粒细胞p-STAT3水平的影响,探讨瘦素在PCOS发病机制中的作用。方法选择行体外受精-胚胎移植(IVF-ET)治疗的肥胖型PCOS患者(肥胖PCOS组)、非肥胖型PCOS患者(非肥胖PCOS组)、排卵功能正常和单纯输卵管因素不育的肥胖(肥胖对照组)及正常体重妇女(正常对照组)各15例。采用免疫印迹技术检测卵巢黄素化颗粒细胞p-STAT3水平。同时将正常人卵巢黄素化颗粒细胞行体外培养,分别加入不同浓度的瘦素(0、10、100、1,000 ng/ml)培养48 h,观察瘦素体外对人卵巢黄素化颗粒细胞p-STAT3水平的影响。结果(1)肥胖型PCOS组、肥胖对照组、非肥胖PCOS组和正常对照组卵巢黄素化颗粒细胞p-STAT3水平分别为(24.28±0.51)、(21.31±1.32)、(11.69±0.67)、(9.03±0.20),实验组间比较有显著性差异(P<0.05),其中肥胖型PCOS组p-STAT3表达水平最高,其次依次为肥胖对照组、非肥胖PCOS组和正常对照组。各组之间两两比较,均有显著性差异(P<0.05)。(2)加入瘦素培养48 h后,卵巢黄素化颗粒细胞p-STAT3水平随瘦素浓度升高而增高,呈浓度依赖性,至瘦素浓度达到100 ng/ml时,p-STAT3水平达到高峰,随后呈下降趋势。结论瘦素通过介导JAK2/STAT3信号途径可能参与了肥胖型PCOS的发病机制。     

肠道菌群在多囊卵巢综合征中作用的研究进展

多囊卵巢综合征(PCOS)是育龄期女性最常见的生殖内分泌疾病,主要特征为排卵功能障碍、卵巢多囊样改变和高雄激素血症。此外,临床上PCOS还常伴随肥胖和胰岛素抵抗。PCOS的临床特征具有复杂性和异质性,其发病机制一直是该领域的研究热点。近年来多项研究发现,PCOS发生发展与肠道菌群密切相关。在PCOS患者以及多种PCOS动物模型中,肠道菌群均发生改变,而菌群的改变与雌、雄激素水平、免疫和代谢异常有一定相关性。因此,本文主要从性激素合成、免疫和代谢三个方面阐述肠道菌群参与PCOS发生发展过程的分子机制,以期为PCOS的诊断和治疗提供一定参考。     

复方醋酸环丙孕酮治疗多囊卵巢综合征伴不育

多囊卵巢综合征 ( PCOS)伴不育 ,氯酚( CC)治疗虽使部分患者恢复排卵 ,但仍有部分患者存在 CC抵抗 ,而复方醋酸环丙孕酮( CPA)可通过抑制黄体生成素 ( L H)减少卵巢雄性激素的分泌 ,阻断外周靶器官雄激素的作用 ,使患者对促排卵药的敏感性增强 ,并能改善雄激素症候群。现已用于 PCOS的前期治疗 [1] ,效果显著。一、资料与方法1 .研究对象 :2 0 0 0年 9月至 2 0 0 1年 1 2月 ,我院生殖中心门诊对 46例 PCOS伴不育患者进行诊治。患者主要表现为 L H升高 ,黄体生成素 /卵泡刺激素 ( L H/ FSH)比值≥ 2 [2 ] ,睾酮( T)升高 ,少数…     

腹腔镜治疗多囊卵巢综合征

1简介 多囊卵巢综合征（polycystic ovarian syndrome,PCOS）是一种常见的内分泌疾病,在育龄期女性中的发病率为6％～8％,是导致无排卵性不孕最常见的原因（约75％）。诊断依据临床表现（肥胖、月经稀发／闭经,多毛）,生化改变（血清黄体生成素及雄激素水平升高）及超声影像特点（卵巢多囊样增大）。PCOS患者还可能存在胰岛素抵抗及代偿性的高胰岛素血症。     

多囊卵巢综合征患者身体成分分析的临床价值

目的通过对多囊卵巢综合征(PCOS)患者进行身体成分分析,评判患者的体型、脂肪分布及营养状况,为PCOS患者的健康管理及并发症的预防提供依据。方法收集2018年6月至2019年8月在江苏省人民医院妇科内分泌门诊就诊的PCOS患者123例为PCOS组,选择同期就诊、月经正常的女性121例为对照组。记录所有研究对象的年龄、身高、体重等参数,采用人体成分分析仪(InBody S10),以生物电阻抗法为原理进行相关指标的测定。比较两组对象一般情况及检测指标的差异,并根据BMI进一步行分层分析。结果两组对象年龄、身高、体重比较均无统计学差异(P均>0.05),PCOS组的BMI[(27.14±4.60)vs.(25.82±4.58)kg/m^2]、全身脂肪含量[(26.55±8.67)vs.(24.23±8.36)kg]、内脏脂肪面积[(100.37±29.98)vs.(92.40±29.34)cm^2]和体脂率[(37.03±6.69)%vs.(35.23±7.06)%]均显著高于对照组(P均<0.05)。根据BMI数值进行分层,当BMI<24 kg/m^2时PCOS组的全身脂肪含量[(15.86±4.71)vs.(13.13±3.39)kg]、内脏脂肪面积[(64.65±19.67)vs.(55.09±13.96)cm^2]和体脂率[(29.10±5.84)%vs.(25.31±4.82)%]亦显著高于对照组(P均<0.05);两组患者细胞外水分率、骨骼肌及骨矿物质含量比较无显著性差异(P均>0.05)。当BMI≥24 kg/m^2时,PCOS组的全身脂肪含量[(29.85±6.73)vs.(27.89±5.91)kg]、内脏脂肪面积[(111.39±23.28)vs.(104.71±21.64)cm^2]亦显著高于对照组(P均<0.05);两组患者体脂率、细胞外水分率、骨骼肌及骨矿物质含量比较无显著性差异(P均>0.05)。结论PCOS患者中超重和肥胖,尤其是腹型肥胖的发生率较高,且无论PCOS患者体重是否正常,全身脂肪含量及内脏脂肪面积均明显高于正常女性。因此,建议对PCOS患者进行体脂及相关指标等检测,以更好地指导临床进行营养与运动管理,改善PCOS患者的体脂分布及比例,有利于改善临床症状及预防远期并发症。     

Abdominal obesity: a health threat

Abdominal obesity is often associated with a constellation of comorbidities that include central adiposity, insulin resistance, dyslipidemia, and hypertension. Clinical evaluations should include a measurement of waist circumference, which is a good marker of abdominal obesity. Abdominal obesity is closely associated with an elevated outflow of free fatty acids from the visceral fat compartment and dysregulation of adipokine expression, accompanied by increased inflammation. The most serious consequences of abdominal obesity are coronary heart disease and stroke. It is also associated, however, with polycystic ovary syndrome and hepatic steatosis. Weight reduction and increased physical activity should be recommended to patients with a high waist circumference. Patients with abdominal obesity and other classic risk factors are at high cardiovascular risk and require strict monitoring of their blood pressure, LDL-c, and blood glucose. New pharmacological strategies might help manage both abdominal obesity and its metabolic consequences.     

Role of insulin and insulin resistance in androgen excess disorders

Insulin has complex effects on cell growth, metabolism and differentiation, and these effects are mediated by a cell-surface bound receptor and eventually a cascade of intracellular signaling events. Among the several metabolic and growth-promoting effects of insulin, insulin resistance is defined as an attenuated effect of insulin on glucose metabolism, primarily the limited export of blood glucose into skeletal muscle and adipose tissue. On the other hand, not all the signaling pathways and insulin-responsive tissues are equally affected, and some effects other than the metabolic actions of insulin are overexpressed. Ovaries and the adrenal glands are two examples of tissues remaining sensitive to insulin actions where insulin may contribute to increased androgen secretion. Polycystic ovary syndrome (PCOS) is the most common form of androgen excess disorder (AED), and its pathogenesis is closely associated with insulin resistance. Patients with idiopathic hirsutism also exhibit insulin resistance, albeit lower than patients with PCOS. Although it is not as evident as in PCOS, patients with congenital adrenal hyperplasia may have insulin resistance, which may be further exacerbated with glucocorticoid overtreatment and obesity. Among patients with severe insulin resistance syndromes, irrespective of the type of disease, hyperinsulinemia promotes ovarian androgen synthesis independently of gonadotropins. It is highly debated in whom and how insulin resistance should be diagnosed and treated among patients with AEDs, including PCOS. It is not suitable to administer an insulin sensitizer relying on only some mathematical models used for estimating insulin resistance. Instead, the treatment decision should be based on the constellation of the signs, symptoms and presence of obesity; acanthosis nigricans; and some laboratory abnormalities such as impaired glucose tolerance and impaired fasting glucose.     

肥胖对胃癌患者术后短期结局的影响

目的探讨肥胖对胃癌患者手术操作及术后短期结局的影响。方法将2006年1月至2008年6月青岛大学医学院附属医院经手术治疗的胃癌患者426例,按入院时人体质量指数（BMI）分为肥胖组（127例,BMI大于或等于25）与非肥胖组（299例,BMI小于25）,予以CT测量脐水平腹部皮下脂肪（SCF）厚度、腹部前后径（APD）和腹部横径（TD）,记录手术时间、术中出血量、术后发热天数、术后腹腔引流量、术后并发症发生率、住院死亡率和住院时间及住院费用．并进行统计学分析。结果胃癌患者中肥胖并发率为29．8％。肥胖组和非肥胖组SCF分别为（21．8±7．1）mm和（14．4±7．5）mm;APD分别为（223．2±24．6）mm和（181．8±23．5）mm,TD分别为（323．6±23．8）mm和（285．8±24．4）mm,差异均具有统计学意义（P=0．000）。肥胖组和非肥胖组的手术时间分别为（182．6±100．4）min和（157．1±46．2）min（P=0．007）;淋巴结清扫数目分别为（17．0±9.3）枚和（21．7±10．9）枚（P=0．000）;术后发热时间分别为（3．0±1．4）d和（2．4±1．4）d（P=0．000）：术后并发症发生率分别为22．8％和12．0％（P=0．005）;住院时间分别为（17．4±12．9）d和（15．0±9．0）d（P=0．029）。两组住院死亡率差异无统计学意义（P=0．702）。结论CT扫描可直观显示胃癌患者的腹部形态．有助于判断手术的难度。肥胖可使胃癌手术操作难度和术后并发症发生率增加．影响其术后短期结局。     

代谢异常对结直肠癌发病的影响

代谢异常与结肠癌的发病有关.代谢综合征是一系列代谢异常症候群.目前国际定义的代谢综合征的几个关键因素,如腹型肥胖、血脂异常、血压升高、糖代谢异常,均与结直肠癌的发病相关.腹型肥胖与糖代谢异常可能是影响直肠癌发病的首要因素.在生理学上,内脏脂肪比皮下脂肪更活跃,并且能生成并分泌激素、细胞因子,参与炎症、代谢以及潜在致癌风险,因此,内脏脂肪的多少可能直接或间接地与结直肠癌的发生相关.肥胖可以通过高胰岛素血症、胰岛素样生长因子和脂肪细胞因子浓度的改变等几种机制增加结直肠癌发病的风险.上述代谢标志物不仅能够从病因学上进一步增进对结直肠癌的了解,也能够探索出与结直肠癌发病风险相关的新肥胖表型.     

多囊卵巢综合征与复发性流产的研究进展

复发性流产(RSA)的发生与多种因素相关,包括年龄、遗传、内分泌与代谢障碍、免疫因素、子宫发育异常、血栓形成倾向、感染、精液质量和生活方式等。多囊卵巢综合征(PCOS)是一种以持续性无排卵、多卵泡不成熟、雄激素水平升高和胰岛素抵抗为主要特征的生殖功能障碍与糖代谢异常并存的内分泌紊乱综合征。PCOS患者RSA的发生率明显高于普通人群,30%~40%的PCOS患者存在自然流产史。目前,PCOS患者易发生RSA的具体发病机制尚不明确,可能与高黄体生成素血症、高雄激素血症、胰岛素抵抗、肥胖、高泌乳素血症、黄体功能不全、血栓形成等有关。本文从上述方面对PCOS患者发生RSA的常见原因及其预防进行综述。     

Effect of Abdominal Obesity on Insulin Resistance and the Components of the Metabolic Syndrome: Evidence Supporting Obesity as the Central Feature

Background: Metabolic syndrome includes abdominal obesity, diabetes type 2, hypertension, dyslipidemia, derangements of fibrinolysis, and atherosclerosis. Since abdominal obesity is one of the major components of the insulin resistance syndrome (IRS), an attempt was made to evaluate the interrelationships between the magnitude of obesity and the components of the syndrome. Methods: A cross-sectional study of 123 subjects with type 2 diabetes, of whom 31 were normal body weight and 92 had varying degrees of obesity was conducted. The participants were investigated in terms of clinical and laboratory findings of IRS. Fasting and 30-min (early) plasma glucose and serum insulin excursions in response to oral glucose challenge (75 g) were determined. The peripheral and hepatic insulin resistance (insensitivity) was calculated by homeostasis model assessment (HOMA). Results: Clinical and biochemical findings were compared with the components of the IRS, and demonstrated that a rise in fasting as well as 30-min insulin secretion increases as abdominal body fat (obesity) increases. There was also a significant and proportional correlation between the magnitude of abdominal obesity and the components of metabolic syndrome. Conclusion: Abdominal adiposity appears to have a pivotal role in the development of IRS.     

腹部皮瓣乳房重建术后并发症及危险因素的研究

目的 探讨腹部皮瓣乳房重建的术后并发症及其相关危险因素.方法 对2001年5月至2008年10月接受腹部皮瓣乳房重建的115例患者的资料和术后并发症情况进行回顾性分析.术后观察指标包括:皮瓣全部坏死、皮瓣部分坏死、脂肪坏死、腹壁疝、腹壁膨出、脂肪液化、感染.并对其术后并发症的相关危险因素进行分析.结果 术后并发症的总发生率为17.4%(20/115),未出现皮瓣全部坏死、腹壁疝、腹壁膨出等严重并发症.皮瓣并发症为脂肪坏死6例(5.2%)、皮瓣部分坏死5例(4.3%)和感染1例(0.9%),供区并发症为脂肪液化8例(7.0%)和感染3例(2.6%).年龄、肥胖和手术时机对于术后并发症的发生率无影响.吸烟者、既往有放疗史者、带蒂横行腹直肌肌皮瓣组术后并发症的发生率较高,但未达到统计学意义.结论 在熟练掌握显微外科技术的情况下,实施腹壁下动脉穿支皮瓣乳房重建更有利于降低术后并发症.术前有吸烟或放疗史的患者应慎重考虑做腹部皮瓣乳房重建,而年龄、肥胖等因素不应成为腹部皮瓣乳房重建的禁忌.     

Increased fat mass compensates for insulin resistance in abdominal obesity and type 2 diabetes: a positron-emitting tomography study

To evaluate the relative impact of abdominal obesity and newly diagnosed type 2 diabetes on insulin action in skeletal muscle and fat tissue, we studied 61 men with (n = 31) or without (n = 30) diabetes, subgrouped into abdominally obese or nonobese according to the waist circumference. Adipose tissue depots were quantified by magnetic resonance imaging, and regional glucose uptake was measured using 2-[(18)F]fluoro-2-deoxyglucose/positron emission tomography during euglycemic hyperinsulinemia. Across groups, glucose uptake per unit tissue weight was higher in visceral (20.5 +/- 1.4 micromol . min(-1) . kg(-1)) than in abdominal (9.8 +/- 0.9 micromol min(-1) . kg(-1), P < 0.001) or femoral (12.3 +/- 0.6 micromol . min(-1) . kg(-1), P < 0.001) subcutaneous tissue and approximately 40% lower than in skeletal muscle (33.1 +/- 2.5 micromol . min(-1) . kg(-1), P < 0.0001). Abdominal obesity was associated with a marked reduction in glucose uptake per unit tissue weight in all fat depots and in skeletal muscle (P < 0.001 for all regions). Recent type 2 diabetes per se had little additional effect. In both intra-abdominal adipose (r = -0.73, P < 0.0001) and skeletal muscle (r = -0.53, P < 0.0001) tissue, glucose uptake was reciprocally related to intra-abdominal fat mass in a curvilinear fashion. When regional glucose uptake was multiplied by tissue mass, total glucose uptake per fat depot was similar irrespective of abdominal obesity or type 2 diabetes, and its contribution to whole-body glucose uptake increased by approximately 40% in obese nondiabetic and nonobese diabetic men and was doubled in obese diabetic subjects. We conclude that 1) in abdominal obesity, insulin-stimulated glucose uptake rate is markedly reduced in skeletal muscle and in all fat depots; 2) in target tissues, this reduction is reciprocally (and nonlinearly) related to the amount of intra-abdominal fat; 3) mild, recent diabetes adds little insulin resistance to that caused by abdominal obesity; and 4) despite fat insulin resistance, an expanded fat mass (especially subcutaneous) provides a sink for glucose, resulting in a compensatory attenuation of insulin resistance at the whole-body level in men.